Contributors JJP was involved in the conception and design of this manuscript and critically revised the draft manuscript. AML designed
and drafted the manuscript. MN provided significant intellectual contribution to the drafting of this manuscript and its revisions.
All the authors read and approved the final manuscript.

After a myocardial infarction (MI), the damaged myocardial tissue is repaired and eventually replaced by scar tissue. In a
substantial proportion of MI patients, the repair mechanisms induce profound structural and functional changes not only in
the infarct zone, but also in the non-infarcted area. These patients show myocardial thinning and expansion of the infarct
zone in the early phase after MI, and pathologic cardiomyocyte hypertrophy, apoptosis and extracellular matrix remodelling
in the remote zone, a process that may continue for months. These underlying mechanisms induce alterations of the left ventricular
(LV) shape, mass, volume, and function, which is also referred to as adverse LV remodelling (figure 1). Although some of these
changes may be adaptive and physiological as short term compensation for the sudden loss of contractile function in the infarcted
area, it may lead over time to heart failure and cardiac death.w1

Figure 1

Adverse Left ventricular (LV) remodelling after myocardial infarction (MI) is characterised by an altered LV shape and LV
volume. Cardiovascular magnetic resonance (CMR) images of a 44-year-old male patient with a large acute anterior MI. Left
panels show the vertical long axis end-diastolic cine image, 3 days (panel A) and 3 months after MI (panel C). The right panels
demonstrate the corresponding late gadolinium enhancement images with the infarct zone and remote zone (panels B and D). At
day 3 after MI, there was extensive microvascular obstruction (panel B, white asterisk) indicated by the black hypoenhanced
areas within the hyperenhanced infarcted myocardium. At 3 months after MI, CMR demonstrated an increase …